Hospital to pilot test that ‘will save lives’

 Ask your competent? doctor to report back when this is written up in protocol format and delivered AND IMPLEMENTED!

Hospital to pilot test that ‘will save lives’

A rapid stroke test that can show whether a common drug will work is being piloted at a new Nottingham clinic.

The cheek swab test is being offered at Queen’s Medical Centre, where a new clinic is assessing and treating patients after suspected minor stroke.

It can show within hours whether a patient carries a genetic variation that affects how well they respond to clopidogrel, the most commonly used drug to treat strokes.

A stroke affects about 100,000 people a year in the UK and happens when a clot blocks blood supply to part of the brain, potentially causing serious or fatal damage.

The pilot is focused on patients suspected of having a transient ischaemic attack, or TIA, often described as a mini-stroke.

A TIA is caused by a temporary disruption in blood flow to the brain and can be a warning sign of a more serious stroke.

Dr Kailash Krishnan, head of stroke medicine at Nottingham University Hospitals NHS Trust, said: “This rapid test can be done in the hospital while we are carrying out other brain and neck scans, and allows us to make the changes to the patient’s treatment all on the same day.

“We can, therefore, be confident that this test will save lives.

“The results could also have huge ramifications for other treatment the patient is receiving, as medications which may not be working for them because of their genetic variation, can also be adjusted.”

The test may also show whether other medicines are working effectively, including warfarin, some antidepressants, drugs used for anxiety or indigestion, and some statins.

The service, which sees around 200 patients a month, will now offer clinic rooms, greater privacy and a calmer environment, staff said.

The purpose-built clinic is open seven days a week.

The pilot is believed to be the first of its type in the UK.

The test identifies whether a patient has a CYP2C19 gene variation, which affects how the body responds to clopidogrel.

The variation is seen in one in three people nationally, and double that in some ethnic groups.

Nottingham University Hospitals NHS Trust said people with changes in the CYP2C19 gene may not respond properly to clopidogrel and are twice as likely to have further strokes when treated with it.

A test for the gene variation already exists, but results can take up to a week.

Doctors said faster testing is important because TIAs can come before larger and more dangerous strokes.

Rashaad Ashraf Ali had a stroke affecting his right eye in 2024, followed by another in 2025 that damaged his left eye.

Concerns that his medication was not working were confirmed after he took the new test.

He said: “It’s a big relief, actually. You can take the medication, but if it doesn’t work for you, you may end up getting further strokes.

“So, it is a big relief to identify the problem early and be put on new medication, which hopefully will be working in the future.”

High levels of engagement reduced readmissions, improved outcomes in hemorrhagic stroke

 So create a protocol on this and get it distributed AND implemented in all stroke hospitals. A great stroke association  would be doing that, but since we have fucking failures of stroke associations  nothing will be done.

High levels of engagement reduced readmissions, improved outcomes in hemorrhagic stroke

High levels of patient engagement with nurse navigators after hospitalization for hemorrhagic stroke led to less disability and lower readmission rates after 90 days, according to research presented at International Stroke Conference.

Researchers at Allegheny Health Network in Pittsburgh aimed to evaluate whether engagement with nurse navigators affected readmissions and outcomes in patients with hemorrhagic stroke.

A study showed that high patient engagement with nurse navigators following hospitalization for hemorrhagic stroke improved outcomes and reduced readmission after 90 days. Image: Adobe Stock

They conducted a retrospective study of patients from seven hospitals from January 2021 to April 2022 and enrolled 368 individuals, of whom 281 were included in analysis (217 with intracerebral hemorrhage and 64 with subarachnoid hemorrhage).

Navigators contacted patients to discuss care and medications, confirm appointments and provide education via phone or virtual encounters. Engagement was defined as low (< 5 encounters) or high ( 5 encounters) over a 90-day period.

The primary outcome was readmission within 90 days, and secondary outcomes included attendance of neurology visit, new or worsening symptoms and 90-day modified Rankin Scale (mRS) score.

According to results, 144 patients were less engaged and 137 were highly engaged. Those who were highly engaged were less likely to be readmitted compared with less engaged patients (23% vs. 42%; adjusted OR = 0.49; 95% CI, 0.28-0.87).

Researchers also reported that highly engaged patients had reduced disability at 90 days compared with less engaged patients (median mRS = 2 vs. 3; aOR = 0.49; 95% CI, 0.3-0.81). However, no differences were reported in engagement and appointment attendance (aOR = 1.73; 95% CI, 0.96-3.11) or new neurologic events (aOR = 0.52; 95% CI, 0.25-1.08).

“Highly engaged patients discharged to a health care facility were also less likely to be readmitted and had less disability at 90 days compared to less engaged patients,” Nicole Dellostretto, LPN, stroke nurse navigator at Allegheny General Hospital, and colleagues wrote.

Does Additional MRI Help CT-Diagnosed Stroke Patients?

WHOM  is going to take this new information, update the protocols on it, AND GET IT DISTRIBUTED AND IMPLEMENTED IN ALL STROKE HOSPITALS?  NO ONE? Then we have no one in stroke with any competence at all. 

Does Additional MRI Help CT-Diagnosed Stroke Patients?

— Investigators acknowledge MRI's value in various circumstances

by Nicole Lou, Senior Staff Writer, MedPage Today July 21, 2022

Patients with acute ischemic stroke (AIS) did not have worse outcomes when a CT-only imaging strategy determined the course of their treatment, according to a small observational study.

Those skipping MRI met the -7.50% threshold for noninferiority, even faring numerically better in rates of death and impaired functional status at hospital discharge compared with propensity-matched peers who had undergone subsequent MRI (modified Rankin Scale score of 3-6: 42.3% vs 48.0%), reported William Powers, MD, of Duke University Medical Center in Durham, North Carolina.

Similarly, noninferiority was supported by the longer-term outcome of stroke or death at 1 year among those discharged alive (19.5% with MRI vs 12.5% without; relative risk 1.14, 95% CI 0.86-1.50), meeting the 0.725 relative risk criterion, the authors noted in JAMA Network Open.

These results suggest that costly routine MRI may not be justified in this setting, despite its wide prevalence.

Powers and colleagues based the study on 123 matched pairs of initially CT-imaged stroke patients with and without additional MRI at the UNC Hospitals Comprehensive Stroke Center.

"Our data strictly apply to the use of MRI in addition to an initial CT in patients hospitalized with AIS and not to other situations for which MRI may be used, such as choice of initial imaging, transient ischemic attacks, uncertain diagnoses, and in persons awakening with stroke symptoms," they cautioned.

What's more, only 6.5% of matched patients underwent endovascular treatment.

"Further research is needed to determine which patients hospitalized with AIS benefit from MRI," Powers and team noted. "More than 90% of patients with AIS receive MRI in addition to CT with few data to determine whether there is an associated benefit with patient outcomes."

In an invited commentary, Michael Teitcher, MD, and Jose Biller, MD, both of Loyola University Chicago Stritch School of Medicine in Maywood, Illinois, called the implications of this study "substantial."

"As stewards of health care resources, clinicians should be asking whether the additional information provided by diagnostic tests meaningfully affects patient outcomes," they wrote.

MRI is thought to have added value for the selection of treatment, and is currently recommended by American stroke guidelines as a reasonable choice after initial imaging of the head in cases where the initial scan did not show infarction or did not provide enough information.

"Of course, there are circumstances in which additional MRI is still justified. But at a minimum, these results should give the health care practitioners reason to pause and reconsider routine use of CT plus MRI," Teitcher and Biller urged.

On the other hand, Bruce Campbell, PhD, of Royal Melbourne Hospital in Australia, argued that "asking whether the imaging alters mortality may not be the right question."

"In the case of MRI after stroke, it may be to confirm the diagnosis, clarify stroke localization (e.g., to confirm likelihood of a stenosis being symptomatic), provide hints of stroke causes, determine timing of anticoagulation, assess the severity of underlying small vessel disease, or assess prognosis," he wrote in a separate editorial.

"Asking any of these valid clinical questions may help improve clinical care by targeting subsequent therapies most appropriately," he noted.

Campbell added that very few proven stroke interventions significantly reduce death, going only so far as to reduce disability or recurrent stroke. "It should therefore not be surprising that a diagnostic test performed during the acute admission would have no association with mortality," he pointed out.

This retrospective observational study relied on electronic medical records of adults hospitalized with AIS who had their admission diagnosis based on CT. Admissions were limited to those from January 2015 to December 2017.

From 508 eligible patients, 246 were selected for propensity-matched analysis. Median age was 68 years, and 53% were men. The two study groups were well matched, except for differences in history of coronary artery disease and chronic kidney disease.

At the UNC stroke center, admission diagnosis was made by the center's neurology resident on call. Residents could order MRI on their own without prior attending consultation. For 111 of the 123 MRIs, there was no specified indication other than stroke or neurological symptoms.

"Data are from a single tertiary referral academic medical center with continuous coverage by in-house neurology residents and subspecialty-trained vascular neurologists. Our findings may not be generalizable to other settings," Powers and colleagues acknowledged.

Furthermore, the nonrandomized study design left room for unmeasured confounding and bias.

Teitcher and Biller called for future prospective studies on the benefit of MRI in stroke, while Campbell warned that "the practicality of obtaining such evidence is less certain, given the potentially very large sample sizes required to address small minimally important clinical differences and confounding variables."

• 

  Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow

Disclosures

Powers and co-authors reported no disclosures.

Teitcher, Biller, and Campbell reported no disclosures.

Primary Source

JAMA Network Open

Source Reference: Cabral Frade H, et al "Comparison of outcomes of ischemic stroke initially imaged with cranial computed tomography alone vs computed tomography plus magnetic resonance imaging" JAMA Netw Open 2022; DOI: 10.1001/jamanetworkopen.2022.19416.

Secondary Source

JAMA Network Open

Source Reference: Teitcher M, Biller J "Understanding the value of diagnostic imaging in ischemic stroke outcomes" JAMA Netw Open 2022; DOI: 10.1001/jamanetworkopen.2022.23077.

Additional Source

JAMA Network Open

Source Reference: Campbell BCV "The value of diagnostic imaging in stroke -- are we asking the right question?" JAMA Netw Open 2022; DOI: 10.1001/jamanetworkopen.2022.23074.

Inhibition of glial D-serine release rescues synaptic damage after brain injury

Now we just need someone to put this together into a protocol and distribute it effectively to all stroke hospitals(meaning the stroke hospital implements the protocol). That will never occur, we have NO leadership that will ensure it gets done.

Inhibition of glial D-serine release rescues synaptic damage after brain injury

Stephen A. Tapanes1| Dena Arizanovska1| Madelen M. Díaz1|Oluwarotimi O. Folorunso2,3| Theresa Harvey3| Stephanie E. Brown3|Inna Radzishevsky4| Liesl N. Close1| Jonathan R. Jagid1|Joacir Graciolli Cordeiro1| Herman Wolosker4| Darrick T. Balu2,3| Daniel J. Liebl1

1The Miami Project to Cure Paralysis,Department of Neurological Surgery,University of Miami Miller School of Medicine,Miami, Florida, USA2Department of Psychiatry, Harvard MedicalSchool, Boston, Massachusetts, USA3Translational Psychiatry Laboratory, McLeanHospital, Belmont, Massachusetts, USA4Department of Biochemistry, RappaportFaculty of Medicine, Technion-Israel Instituteof Technology, Haifa, IsraelCorrespondenceDaniel J. Liebl, The Miami Project to CureParalysis, The University of Miami, 1095 NW14th Terrace, R-48, Miami, FL 33136, USA.

Abstract 

Synaptic damage is one of the most prevalent pathophysiological responses to traumatic CNS injury and underlies much of the associated cognitive dysfunction;however, it is poorly understood. The D-amino acid, D-serine, serves as the primary co-agonist at synaptic NMDA receptors (NDMARs) and is a critical mediator of NMDAR-dependent transmission and synaptic plasticity. In physiological conditions,D-serine is produced and released by neurons from the enzymatic conversion of L-serine by serine racemase (SRR). However, under inflammatory conditions, glial cells become a major source of D-serine. Here, we report that D-serine synthesized by reactive glia plays a critical role in synaptic damage after traumatic brain injury (TBI) and identify the therapeutic potential of inhibiting glial D-serine release though the transporter Slc1a4 (ASCT1). Furthermore, using cell-specific genetic strategies and pharmacology, we demonstrate that TBI-induced synaptic damage and memory impairment requires D-serine synthesis and release from both reactive astrocytes and microglia. Analysis of the murine cortex and acutely resected human TBI brain also show increased SRR and Slc1a4 levels. Together, these findings support a novel role for glial D-serine in acute pathological dysfunction following brain trauma,whereby these reactive cells provide the excess co-agonist levels necessary to initiate NMDAR-mediated synaptic damage.